Non-ST elevation Myocardial Infarction or Non-STEMI
I. What every physician needs to know.
Non-ST-segment elevation myocardial infarction (formerly known as non-Q-wave myocardial infarction MI) is an acute coronary syndrome caused by myocardial ischemia which results clinically in angina (or its equivalent) elevation of cardiac biomarkers indicating myocardial necrosis and generally involves electrocardiogram (EKG) findings of ST segment depressions or T wave inversions. Myocardial ischemia develops as a result of an imbalance between myocardial oxygen supply and demand and is most commonly due to disruption of an atherosclerotic plaque.
In contrast to a ST-segment elevation myocardial infarction (STEMI), which results from a total occlusion of a segment(s) of the coronary arteries, a NSTEMI is often the result of subtotal coronary artery occlusion. It is initially difficult to distinguish NSTEMI from unstable angina at the time of symptom onset. Confirmation of a NSTEMI is made by the presence of an elevation in cardiac biomarkers.
II. Diagnostic Confirmation: Are you sure your patient has Non-STEMI?
A. History Part I: Pattern Recognition:
The typical presentation is >10 minutes of substernal, pressure-like chest pain radiating to the shoulder, neck, jaw, or left arm. However, pain can be felt isolated to any of these areas and sometimes no pain is felt at all. Most often occurring at rest, the pain is more intense or prolonged than any previously experienced episodes of unstable angina, usually lasting more than 20 minutes. Associated symptoms include diaphoresis, nausea/vomiting (especially with inferior wall involvement), or lightheadedness. Occasionally location of pain may be epigastric and easily confused for gastrointestinal (GI) illnesses.
In the absence of chest pain, unexplained dyspnea is worrisome and should be considered an anginal equivalent, particularly in patients with risk factors for atherosclerotic cardiovascular disease (ASCVD).
Atypical presentations or “silent myocardial infarctions (MIs)” more commonly occur in females, elderly, diabetics, and patients with prior heart failure. Up to 33% of patients having a myocardial infarction present with symptoms other than chest pain.
B. History Part 2: Prevalence:
Risk factors for Coronary Heart Disease (CHD):
Hypertension: BP >140/90 mmHG (millimeters mercury) or use of antihypertensive meds.
Family history in a first degree relative of premature coronary artery disease (men < 55 years old or women < 65 years old).
Dyslipidemia: elevations in non- High density lipoprotein (HDL) cholesterol and low levels of HDL cholesterol.
Age: males ≥ 55 years old and females ≥ 65 years old.
Diabetes mellitus (DM).
Microalbuminuria or estimated GFR < 60 mL/min (milliliters/minute).
Lifestyle factors such as tobacco smoking, alcohol intake, obesity (BMI>30 kilograms/meter2 [kg/m2]), physical inactivity and diet.
An HDL > 60 mg/dl (milligrams/deciliter) is a negative risk factor for ASCVD.
Coronary heart disease risk equivalents include:
Non-coronary atherosclerotic disease – carotid artery disease, abdominal aortic aneurysm, disease, cerebral vascular and peripheral arterial disease.
Chronic kidney disease.
The risk of having a cardiovascular event in these patients is equivalent to persons with prior history of coronary artery disease (CAD).
C. History Part 3: Competing diagnoses that can mimic Non-STEMI.
Cardiac chest pain:
STEMI – ST elevations noted on EKG with elevated cardiac enzymes; posterior wall MIs are difficult to differentiate from NSTEMI unless posterior leads are placed during EKG recording.
Unstable angina – normal cardiac enzymes; EKG changes (ST depressions or T wave inversions) are usually transient.
Acute pericarditis – concomitant symptoms of viral illness; positional changes in chest pain; diffuse ST-elevation on EKG with PR depressions.
Vasospasm (Prinzmetal’s angina or cocaine-induced).
Myocarditis – chest pain may be sharp, +/- fever, may describe recent symptoms consistent with a viral infection.
Coronary artery dissection (associated with acute coronary syndromes (ACS) in peripartum women).
Aortic dissection – sharp, tearing chest pain without ST elevation on EKG (unless artery dissection occurs). Widened mediastinum on chest X-ray (CXR).
Takotsubo or stress-induced cardiomyopathy – brought on by an emotional or physical stressor.
Non-cardiac chest pain:
GI: gastroesophageal reflux disease (GERD), esophageal spasm, esophageal rupture, pancreatitis, cholecystitis, choledocholithiasis, peptic ulcer disease (PUD).
Pulmonary: pneumonia, pulmonary emboli, tension pneumothorax.
Costochondritis: reproducible chest wall tenderness.
D. Physical Examination Findings.
Presentation can vary widely from a completely normal exam to sudden death resulting from a ventricular arrhythmia.
Tachycardia and/or hypertension can result from reflex activation of the sympathetic nervous system in response to myocardial ischemia. Bradycardia may be present in setting of an inferior wall myocardial infarction due to parasympathetic activation.
A paradoxically split 2nd heart sound or presence of a 3rd or 4th heart sound may be audible.
Pre-existing murmurs may change in intensity or timing. A new murmur of mitral regurgitation could indicate papillary muscle dysfunction.
In large territory infarcts, there may be signs of acute heart failure (e.g., hypotension, pulmonary edema). Hypotension and elevated jugular venous pressure in the absence of pulmonary edema is indicative of a right ventricular infarct.
E. What diagnostic tests should be performed?
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
The general approach to biochemical diagnosis of acute MI is measurement of troponin I or T at 0 hours and 3-6 hours of presentation. If first two values are negative and high index of suspicion for NSTEMI exists, then repeat at 12 to 24 hours. If troponin assay is unavailable, then a less specific and sensitive alternative is to serially measure CK-MB (creatinine kinase myocardial band).
CK-MB – less specific for myocardial injury than cardiac troponins. Elevated CK-MB with normal troponin more often indicates release of MB isoenzyme from noncardiac tissue. The utility of CK-MB is greater than troponins in the diagnosis of post-procedural MIs.
Cardiac troponin (I and T) – more specific and sensitive than CK-MB for diagnosis of myocardial injury, but can be elevated in other conditions. A negative troponin does not exclude MI especially if done soon after symptom onset. Eighty percent of patients with NSTEMI will rule in within 2-3 hours. Serial monitoring of troponin can exclude most acute MIs within 6-8 hours of symptom onset. Levels can stay elevated for 1-2 weeks after an acute MI but do not rapidly rise or fall. Reinfarction can be diagnosed if there is a ≥ 20 % increase in a repeated sample.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
EKG: must be done in the evaluation of a patient with symptoms suggestive of ACS. In NSTEMI, it may reveal ST depressions and/or T wave inversions. These characteristic EKG changes are not required for the diagnosis of an NSTEMI, however, as a normal EKG is found in up to 6% of patients with NSTEMI. ST elevations or pathologic Q waves will be absent.
As opposed to ST segment elevations, which can help to localize the area of myocardium that is infarcting and suggest the involvement of a particular coronary artery, ST depressions and T wave inversions do not localize to an area of the myocardium.
One exception is ST depression in ≥2 precordial leads (V1-V4), which should prompt evaluation for possibility of posterior wall infarction with placement of posterior leads (V7, V8, V9) as this may aid is diagnosing a posterior STEMI.
If the initial EKG is nondiagnostic in a patient with ongoing chest pain with a high index of suspicion for an acute MI, the EKG should be repeated every 20 minutes to evaluate for dynamic EKG changes.
Echocardiogram: to assess for segmental wall motion abnormalities, overall left ventricle function, and for the presence of any valvular abnormalities.
III. Default Management.
A. Immediate management.
For any patient suspected to have NSTEMI, immediately (ideally within 10 mins of arrival) establish intravenous (IV) access, initiate continuous EKG monitoring and obtain 12-lead EKG, obtain blood for cardiac biomarkers, complete blood count (CBC), basic metabolic panel (BMP), and a coagulation profile; prothrombin time (PT), partial thromboplastin time (PTT) and international normalized ratio (INR), and assess for and maintain hemodynamic stability.
Sublingual (SL) nitroglycerin (NTG) 0.4 mg (milligrams) every 5 minutes for 3 times, then given IV for persistent pain, hypertension, or heart failure. NTG is contraindicated if phosphodiesterase inhibitor was used within previous 24 hours, for those patients with right ventricular infarcts and hypotensive patients.
Morphine 2 to 4 mg IV for relief of chest pain that is not relieved by nitroglycerin.
Supplemental oxygen for patients with cyanosis, respiratory distress, or hypoxemia (arterial oxygen saturation < 90%).
If not contraindicated, start beta blockers within the first 24 hours – prevents recurrent ischemia (by treating hypertension and tachycardia, both of which placed an increased demand on an already ischemic myocardium). Rate control also helps prevent ventricular arrhythmias. Verapamil or diltiazem are acceptable alternatives when beta-blockers are contraindicated, but should be avoided in patients with significant left ventricular (LV) dysfunction.
Oral angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) should be given within 24 hours to NSTEMI patients with left ventricular ejection fraction (LVEF) < 40% or evidence of pulmonary congestion.
Discontinue all nonsteroidal anti-inflammatory (NSAIDs) except aspirin (ASA) at time of presentation.
Initiate or continue a high intensity statin.
Quick risk assessment and selection of management strategy
Determination between an early invasive versus a conservative approach to management of NSTEMI is made by risk stratifying for future cardiac events. In addition to the presence of any of the extremely high risk presentations below, calculation of the TIMI (thrombolysis in myocardial infarction) risk score is also useful in assessment of risk.
Extremely high risk clinical presentations of NSTEMI:
Cardiogenic shock or hemodynamic instability.
Severe LV dysfunction or heart failure.
Persistent angina in spite of medical management above.
New (or worsening) mitral regurgitation or new ventricular septal defect.
Sustained ventricular arrhythmia.
These patients should undergo emergent coronary angiography and revascularization.
TIMI risk score (assign one point to each of the factors below that are present):
Age ≥ 65 years;
≥3 risk factors for coronary heart disease (CHD);
History of coronary stenosis of ≥ 50%;
ST segment deviation on EKG;
≥ 2 episodes of angina in past 24 hours;
Elevated serum cardiac biomarkers;
Use of aspirin in the last 7 days.
TIMI Risk Scores: 0-2 low risk, 3-4 intermediate risk, 5-7 high risk of a further cardiac event.
Early (usually < 24 hours) cardiac catheterization with revascularizationis indicated for intermediate and high TIMI risk scores.
A conservative strategy with medical management is considered in patients with low TIMI risk scores.
Antiplatelet and Anticoagulant Therapy
All patients: Unless absolutely contraindicated, all patients with suspected or confirmed NSTEMI should be given non-enteric coated, chewable ASA 162-325 mg immediately on presentation. In patients unable to take ASA, clopidogrel should be used. In the absence of contraindications, all NSTEMI patients should also be started on anticoagulation with unfractionated heparin (UFH), enoxaparin, or fondaparinux. If an invasive approach is planned, the anticoagulant bivalirudin can be used.
If a conservative, noninvasive approach is planned, load with clopidogrel or ticagrelor and continue maintenance dose for a minimum of 1 month, but ideally up to 1 year. Patients who are initially treated conservatively with medical management should undergo stress testing to further stratify need for inpatient versus outpatient angiography.
In all patients with NSTEMI if an early invasive strategy is planned add a P2Y12 inhibitor medication such as clopidogrel, prasugrel or ticagrelor; ASA; and anticoagulation. For those patients with intermediate to high-risk features, a GP IIb/IIIa inhibitor, such as eptifibatide and tirofibran should be considered.
Fibrinolytics should not be used in patients with NSTEMI.
Revascularization: Selection of either PCI or CABG (coronary artery bypass graft) for revascularization after angiography largely depends on extent/severity of the coronary arteries involved.
Maintaining potassium and magnesium concentrations above 4.0 meq/L (milliequivalents/liter) and 2.0 meq/L respectively is recommended as prophylaxis for life-threatening ventricular tachyarrhythmias.
B. Physical Examination Tips to Guide Management
Vital signs should be checked frequently to assess for developing hemodynamic compromise (e.g., arrhythmias or hypotension from cardiac tamponade, heart failure or right ventricular infarcts). Monitor heart and lung sounds for new murmurs or signs of heart failure. A mitral regurgitation (MR) murmur may develop post-infarction. A new or worsening MR occurring concurrently with hypotension and signs of pulmonary edema is indicative of life-threatening papillary muscle rupture. Presence of a pericardial friction rub heard on auscultation post-MI could represent peri-infarction pericarditis.
C. Laboratory Tests to Monitor Response to, and Adjustments in, Management.
Serial cardiac biomarkers should be measured until they peak and start to trend down. If recurrence of chest pain, repeat biomarkers to assess for re-infarction.
CBC: anemia can result in decreased oxygen supply to myocardium and subsequent ischemia. Although there are differing opinions about when to transfuse, it’s probably more beneficial than risky to give a packed red blood cell (PRBC) transfusion if the hemoglobin level is < 8mg/dL. Monitor for decreases in hemoglobin or hematocrit while on antiplatelets or anticoagulation.
Monitor PT/INR/PTT while on warfarin or unfractionated heparin.
BMP: creatinine and potassium levels should be monitored after initiating ACE inhibitor. Potassium and magnesium should be replaced as above.
Blood glucose should be measured pre-meal to tailor insulin regimens to achieve adequate glycemic control. Ideally blood glucose levels should be kept below 180 mg/dL.
D. Long-term management.
An echocardiogram should be performed to assess LV function in those who haven’t undergone angiography or left ventriculography.
Initiate or continue medications that have proven mortality benefits (recommendations below are based on absence of contraindications):
Medically managed patients without stenting: clopidogrel 75 mg daily or ticragelor 90 mg twice daily (for at least 1 month and ideally up to 1 year) and aspirin 75 to 162 mg indefinitely.
Patients who received a bare-metal stent (BMS) or a drug-eluting stent (DES): clopidogrel 75 mg daily, prasugrel 10 mg daily or ticagrelor 90 mg twice daily (for 1 year) and aspirin 81-325 mg daily indefinitely. Continuation of dual antiplatelet therapy past 12 months should be considered in patients that have not had adverse events. In patients with BMS who have had a bleeding complication consideration can be given to discontinuing the P2Y12 inhibitor after 1 month as the risk of stent thrombosis is the greatest in the first 14-30 days.
ACE inhibitor (or ARB) should be given within 24 hours of diagnosis and continued indefinitely (particularly if pt has hypertension [HTN], DM, heart failure [HF], or LV dysfunction with EF ≤ 40%). Use should be avoided in patients with hypotension, hyperkalemia, bilateral renal artery stenosis or renal impairment.
Beta blockers should be started ideally within 24 hours of the acute event and continued indefinitely. This medication class should be used with caution in patients with signs of heart failure, cardiogenic shock, conduction abnormalities or reactive airway disease
Statins should be given to all post-NSTEMI patients regardless of LDL. For patients ≤ 75 years a high intensity statin (atorvastatin 40-80mg or rosuvastatin 20-40mg) should be used.
For patients > 75 years or patients who are intolerant to a high intensity statin, moderate intensity statin should be used.
Aldosterone antagonists are recommended for use in NSTEMI patients who are already taking therapeutic doses of an ACE inhibitor, have DM, LV dysfunction (with an EF ≤ 40%), or have symptomatic heart failure. Use should be avoided in patients with hyperkalemia or renal impairment.
Control symptoms of ischemia with nitroglycerin and beta blockers (or calcium channel blockers).
Oral anticoagulation with warfarin is recommended to prevent embolization in the setting of atrial fibrillation or presence of an LV thrombus. Anticoagulation with one of the novel oral anticoagulants (dabigatran, rivaroxaban, apixaban and edoxaban) may be considered for patients.
Recommend lifestyle and risk factor modification:
Encourage smoking cessation. If needed, start nicotine or non-nicotine replacement therapy.
HTN – “Joint National Committee 8” guidelines recommend goal blood pressure less than 150/90mmHg in patients ≥ 60 years of age and less than140/90mmHg in patients with. For DM and chronic kidney disease (CKD) regardless of age as well as patients < 60 years old.
DM – dietary and medication regimens modified to achieve HgbA1c < 7%.
Dyslipidemia – statin therapy is the mainstay of treatment.
Dietary – reduce intake of saturated and trans fats, cholesterol, sodium, sweets, sugar-sweetened beverages and red meats. Increase intake of fresh fruits, vegetables, whole grains, and low-fat dairy, poultry, fish, legumes, nontropical vegetable oils and nuts.
Promote an average of 40 minutes of moderate to vigourous physical activity at least 3-4 days per week. Patients can usually start exercising 1 to 2 weeks after NSTEMI.
Weight recommendations: BMI 18.5 to 24.9 kg/m2 and waist circumference < 40 inches for men and < 35 inches for women.
IV. Management with Co-Morbidities.
A. Renal Insufficiency.
Use of isosmolar contrast agents is indicated for patients with CKD who require angiography. Dose adjustments should be made for medications that are renally cleared.
B. Liver Insufficiency.
No change in standard management.
C. Systolic and Diastolic Heart Failure.
No change in standard management.
D. Coronary Artery Disease or Peripheral Vascular Disease.
No change in standard management.
E. Diabetes or other Endocrine issues.
Diabetes is an independent predictor of adverse cardiac events. Diabetics with NSTEMI should receive an intravenous GP IIb/IIIa inhibitor.
Diabetic patients with acute MI require aggressive glycemic management with goal blood glucose <180 mg/dL. Caution should be taken to avoid hypoglycemia. It may be necessary to administer insulin therapy to achieve these goals.
In cases of active or inoperable terminal cancer, discuss with the patient risks and benefits of invasive coronary revascularization and consider conservative medical management.
G. Immunosuppression (HIV, chronic steroids, etc).
No change in standard management.
H. Primary Lung Disease (COPD, Asthma, ILD).
Beta blockers should be used with caution in patients with asthma. Acceptable alternatives for anti-ischemic therapy in these patients are the non-dihydropyridine calcium channel blockers, verapamil or diltiazam, however, these medications should be avoided in patients with impaired left ventricular systolic function.
I. Gastrointestinal or Nutrition Issues.
In patients with pre-existing peptic ulcer disease (PUD) or history of a gastrointestinal (GI) bleed, use caution with anticoagulation and antiplatelet therapy and monitor for GI bleed. It’s reasonable to initiate a proton pump inhibitor (PPI) for GI prophylaxis in these cases.
J. Hematologic or Coagulation Issues.
No change in standard management.
K. Dementia or Psychiatric Illness/Treatment.
In patients with advanced dementia, risks versus benefits of performing invasive revascularization should be discussed with the patient’s health care proxy or family members.
V. Transitions of Care.
A. Sign-out considerations While Hospitalized.
Monitor PTT (for UFH), INR (for warfarin) and CBC while on any anticoagulation.
Monitor cardiac biomarkers.
Check creatinine and potassium if ACE inhibitor initiated.
B. Anticipated Length of Stay (LOS).
LOS is dependent on the method of revascularization undertaken. After an uncomplicated PCI, patients can be discharged as early as the next day depending on the patient’s clinical course.
C. When is the Patient Ready for Discharge.
Post-NSTEMI patients should be hemodynamically stable, free of ischemic symptoms, and able to ambulate without triggering symptoms of ischemia prior to discharge. If a conservative medical approach was recommended, they should have undergone risk stratification with stress testing prior to discharge to evaluate need for inpatient coronary angiography.
D. Arranging for Clinic Follow-up.
1. When should clinic follow up be arranged and with whom.
Follow-up with primary care physician and cardiologist within 14 days of discharge or earlier if symptoms of ischemia recur.
2. What tests should be conducted prior to discharge to enable best clinic first visit.
Patients who were initially treated conservatively with medical management should undergo stress testing to further stratify need for inpatient versus outpatient angiography.
3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.
INR for those started on warfarin.
BMP (for creatinine and potassium) for those started on an ACE inhibitor or ARB.
E. Placement Considerations.
Other than placements in nursing home, rehab, or hospice where appropriate, consider referral to a cardiac rehabilitation program. These programs provide a comprehensive approach to risk factor modification, supervised exercise regimens, patient education and counseling. Cardiac rehab programs are beneficial for post-NSTEMI patients with multiple modifiable risk factors.
F. Prognosis and Patient Counseling.
30-day and 1-year mortality after NSTEMI is higher for diabetics (2.1% and 7.2% respectively) as compared to nondiabetics (1.1% and 3.1% respectively).
Patient counseling should include:
Education about symptoms suggestive of worsening myocardial ischemia or MI and advise regarding when to seek emergent medical care.
Prescribing SL NTG on discharge and educating patients on its proper use.
Recommendations for dietary modifications.
Stressing importance of medication compliance.
Recommendations for resuming sexual activity: After uncomplicated MI, sexual activity with the same partner can resume in 7 to 10 days. Phosphodiesterase inhibitors should not be used within 24 to 48 hours of taking nitrates.
Recommendations for driving: return to driving post-MI is dependent on meeting the criteria set forth by the state’s Department of Motor Vehicles (DMV). Driving can begin as early as one week (if all state DMV criteria met) and should be delayed 2-3 weeks after symptoms have resolved in the case of a complicated MI.
Education regarding smoking cessation and avoiding secondhand smoke should also be provided.
VI. Patient Safety and Quality Measures.
A. Core Indicator Standards and Documentation.
JCAHO/Joint Commission measures the following standards of care provided for most patients with a diagnosis of AMI:
Aspirin given within 24 hours of arrival to ED and prescribed at time of discharge.
ACE inhibitor or ARB prescribed for LV systolic dysfunction.
Adult smoking cessation advise or counseling.
Beta blocker on arrival and prescribed at discharge.
Median time to fibrinolysis in STEMI (ideally within 30 minutes of hospital arrival).
Median time to primary PCI (ideally within 90 minutes of hospital arrival for STEMI).
Statin prescribed at discharge.
B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.
Venous thromboembolism prophylaxis: low-dose UFH, enoxaparin, or fondaparinux are indicated for VTE prophylaxis in NSTEMI patients who are anticipated to be on bedrest for more than 24 hours. Unless other risk factors for DVT exist, NSTEMI patients predicted to be on bedrest for less than 24 hours generally don’t require VTE prophylaxis.
Gastrointestinal prophylaxis: single or dual antiplatelet therapy with aspirin and/or a thienopyridine (clopidogrel and especially prasugrel) predispose to GI toxicity. The risk is increased in patients with pre-existing PUD, a history of GI bleed, concurrent use of oral anticoagulation, glucocorticoid use, older age. Proton pump inhibitors should be used for GI prophylaxis in patients who receive antiplatelet therapy and have other risk factors for GI toxicity. Although there is concern for safety in concurrent use of clopidogrel with a PPI, the COGENT trial did not reveal a statistically significant negative impact of omeprazole on cardiovascular events in patients being treated with clopidogrel.
Since 2013, Centers for Medicare and Medicaid Services (CMS) has been penalizing hospitals with higher than expected 30-day readmission rates after MI, by imposing penalties against Medicare payments to the hospital. Strategies to prevent readmission include:
Developing a long-term management plan which includes prescribing on discharge any medications that improve prognosis where applicable (e.g., ACE inhibitor, beta blockers, antiplatelet agents, statins, aldosterone antagonists) and tailoring a regimen aimed at lifestyle and risk factor modification.
Emphasizing the importance of proper use and compliance with medications.
Reconciling medications prescribed at discharge with those being taken on admission.
Effectively communicating the long-term management plan with the patient, outpatient primary care physician, and patient’s cardiologist.
Providing a clear and understandable discharge plan to the patient and outpatient care providers.
Making a follow-up call to the patient within 48 hours of discharge when possible.
Providing referrals to cardiac rehab program where appropriate.
IV. What's the evidence?
Amsterdam, EA, Wenger, NK, Brindis, RG. “2014 ACC/AHA Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes : A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines”. J Am Coll Cardiol. vol. 64. 2014. pp. e139-e228.
James, PA, Oparil, S, Carter, BL. “2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults Report from the Panel Members Appointed to the Eight Joint National Committee (JNC 8)”. JAMA. vol. 311. 2014. pp. 507-520.
Stone, NJ, Robinson, JG, Lichtenstein, AH. “2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults”. Circulation. vol. 129. 2014. pp. S1-S45.
Thygesen, K, Alpert, JS, White, HD. “Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction: Universal definition of myocardial infarction”. Circulation. vol. 116. 2007. pp. 2634-2653.
Jaffe, AS. “Chasing Troponin: How Low Can You Go if You Can See the Rise”. J Am Coll Cardiol. vol. 48. 2006. pp. 1763-1764.
Harrington, RA, Becker, RC, Cannon, CP. “Antithrombotic therapy for non-ST-segment elevation acute coronary syndromes: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)”. Chest. vol. 133. 2008. pp. 670S-707S.
Antman, EM, Cohen, M, Bernink, PJ. “The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making”. JAMA. vol. 284. 2000. pp. 835-842.
Montalescot, G, Dallongeville, J, Belle, EV. “STEMI and NSTEMI: are they so different? 1 year outcomes in acute myocardial infarction as defined by the ESC/ACC definition (the OPERA registry)”. Eur Heart Journal. vol. 28. 2007. pp. 1409-1417.
Kocher, RP, Adashi, EY. “Hospital Readmissions and the Affordable Care Act: Paying for Coordinated Quality Care”. JAMA. vol. 306. 2011. pp. 1794-1795.
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- Non-ST elevation Myocardial Infarction or Non-STEMI
- I. What every physician needs to know.
- II. Diagnostic Confirmation: Are you sure your patient has Non-STEMI?
- A. History Part I: Pattern Recognition:
- B. History Part 2: Prevalence:
- C. History Part 3: Competing diagnoses that can mimic Non-STEMI.
- D. Physical Examination Findings.
- E. What diagnostic tests should be performed?
- III. Default Management.
- A. Immediate management.
- B. Physical Examination Tips to Guide Management
- C. Laboratory Tests to Monitor Response to, and Adjustments in, Management.
- D. Long-term management.
- IV. Management with Co-Morbidities.
- A. Renal Insufficiency.
- B. Liver Insufficiency.
- C. Systolic and Diastolic Heart Failure.
- D. Coronary Artery Disease or Peripheral Vascular Disease.
- E. Diabetes or other Endocrine issues.
- F. Malignancy.
- G. Immunosuppression (HIV, chronic steroids, etc).
- H. Primary Lung Disease (COPD, Asthma, ILD).
- I. Gastrointestinal or Nutrition Issues.
- J. Hematologic or Coagulation Issues.
- K. Dementia or Psychiatric Illness/Treatment.
- V. Transitions of Care.
- A. Sign-out considerations While Hospitalized.
- B. Anticipated Length of Stay (LOS).
- C. When is the Patient Ready for Discharge.
- D. Arranging for Clinic Follow-up.
- 1. When should clinic follow up be arranged and with whom.
- 2. What tests should be conducted prior to discharge to enable best clinic first visit.
- 3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.
- E. Placement Considerations.
- F. Prognosis and Patient Counseling.
- VI. Patient Safety and Quality Measures.
- A. Core Indicator Standards and Documentation.
- B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.